ArticleFrontiers in molecular neuroscience2016
Expression of Tgfβ1 and Inflammatory Markers in the 6-hydroxydopamine Mouse Model of Parkinson's Disease.
Article in Frontiers in molecular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Intracisternal IGF-1 gene delivery attenuates early anxiety-like behavior but not dopaminergic neurodegeneration in a 6-OHDA rat model of parkinsonism.Frontiers in aging neuroscience · 2026Article
- Knockdown of RUNX2 Attenuated A1 Astrocyte Overactivation, Brain Injury, and Cerebral Edema During Ischemic Stroke.Neuromolecular medicine · 2025Article
- NMDA receptor remodeling and nNOS activation in mice after unilateral striatal injury with 6-OHDA.Heliyon · 2024Article
- Neuroprotective effects ofJournal of traditional and complementary medicine · 2024Article
- Characterization of graded 6-Hydroxydopamine unilateral lesion in medial forebrain bundle of mice.Scientific reports · 2024Article
- Selection of suitable reference genes for gene expression studies in HMC3 cell line by quantitative real-time RT-PCR.Scientific reports · 2024Article
- Inhibition of neuroinflammation by GIBH-130 (AD-16) reduces neurodegeneration, motor deficits, and proinflammatory cytokines in a hemiparkinsonian model.Frontiers in neuroanatomy · 2024Article
- The role and potential therapeutic targets of astrocytes in central nervous system demyelinating diseases.Frontiers in cellular neuroscience · 2023Review
- Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases.Biomolecules · 2022Review
- Article
- Developmental pathways linked to the vulnerability of adult midbrain dopaminergic neurons to neurodegeneration.Frontiers in molecular neuroscience · 2022Review
- New models of Parkinson's like neuroinflammation in human microglia clone 3: Activation profiles induced by INF-γ plus high glucose and mitochondrial inhibitors.Frontiers in cellular neuroscience · 2022Article
- Flavonoids, the Family of Plant-Derived Antioxidants Making Inroads into Novel Therapeutic Design Against Ionizing Radiation-Induced Oxidative Stress in Parkinson's Disease.Current neuropharmacology · 2022Review
- Vascular Inflammation Is a Risk Factor Associated with Brain Atrophy and Disease Severity in Parkinson's Disease: A Case-Control Study.Oxidative medicine and cellular longevity · 2020Article
- Time dependent degeneration of the nigrostriatal tract in mice with 6-OHDA lesioned medial forebrain bundle and the effect of activin A on L-Dopa induced dyskinesia.BMC neuroscience · 2019Article
- Therapeutic Effect of Modulating TREM-1 via Anti-inflammation and Autophagy in Parkinson's Disease.Frontiers in neuroscience · 2019Article
- Abrogation of the Circadian Nuclear Receptor REV-ERBα Exacerbates 6-Hydroxydopamine-Induced Dopaminergic Neurodegeneration.Molecules and cells · 2018Article
- Effect of Intrastriatal 6-OHDA Lesions on Extrastriatal Brain Structures in the Mouse.Molecular neurobiology · 2018Article
- Designer exosomes produced by implanted cells intracerebrally deliver therapeutic cargo for Parkinson's disease treatment.Nature communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder that is characterized by loss of midbrain dopaminergic (mDA) neurons in the substantia nigra (SN). Microglia-mediated neuroinflammation has been described as a common hallmark of PD and is believed to further trigger the progression of neurodegenerative events. Injections of 6-hydroxydopamine (6-OHDA) are widely used to induce degeneration of mDA neurons in rodents as an attempt to mimic PD and to study neurodegeneration, neuroinflammation as well as potential therapeutic approaches. In the present study, we addressed microglia and astroglia reactivity in the SN and the caudatoputamen (CPu) after 6-OHDA injections into the medial forebrain bundle (MFB), and further analyzed the temporal and spatial expression patterns of pro-inflammatory and anti-inflammatory markers in this mouse model of PD. We provide evidence that activated microglia as well as neurons in the lesioned SN and CPu express Transforming growth factor β1 (Tgfβ1), which overlaps with the downregulation of pro-inflammatory markers Tnfα, and iNos, and upregulation of anti-inflammatory markers Ym1 and Arg1. Taken together, the data presented in this study suggest an important role for Tgfβ1 as a lesion-associated factor that might be involved in regulating microglia activation states in the 6-OHDA mouse model of PD in order to prevent degeneration of uninjured neurons by microglia-mediated release of neurotoxic factors such as Tnfα and nitric oxide (NO).
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